Cartilage is a stiff yet flexible connective tissue found in many areas in the bodies of humans and other animals, including the joints between bones, the rib cage, the ear, the nose, the elbow, the knee, the ankle, the bronchial tubes and the intervertebral discs.

Joints Anatomy

Cartilage Matrix

Cartilage matrix is a homogeneous material principally composed of proteoglycans, macromolecules with a proteinaceous backbone, to which is attached complex carbohydrates (these carbohydrates are "glycosaminoglycans," usually abbreviated GAGs). The GAGs radiate from the protein core like the bristles of a bottle brush. The principal GAGs of cartilage are chondroitin sulfate and keratan sulfate. Another matrix component is hyaluronic acid, a gelatinous mucopolysaccharide. The hyaluronic acid acts as a sort of cement to bind the proteoglycans together into large aggregates.

As you might expect with this much carbohydrate present, the matrix of cartilage is very strongly positive when stained with the PAS reaction for carbohydrates, but in an H&E stained preparation it's sort of a pale pink to blue color. What little H&E stain is taken up tends to be localized into the chondrocytes, which stand out against the matrix. Notice also in the images above that there's a sort of "ring" of deeper stain close to the chondrocytes. That's where the matrix has just been formed and the density of staining is highest.
Fibers

The fibrillar component of hyaline cartilage consists of a few strands of Type II collagen. Type II fibers (10 to 20 nm diameter) and unbanded. You won't be able to make them out, so don't bother to try. The matrix fills the spaces in the meshwork of Type II fibers.

"Appositional" and "Interstitial" Growth Patterns In Cartilage

An increase in the overall size, or a change in shape of a cartilaginous structure obviously has to happen somehow. Since hyaline cartilage forms the model for the bones of an developing embryo, as the embryo grows in size and develops new parts, the skeletal model has to keep pace with it. This process of growth and reshaping occurs in two ways: interstitial growth and appositional growth.

The only significant difference in the two processes is where they occur. Appositional growth takes place "at the edge" of the cartilage mass (i.e., between the cartilage proper and the surrounding perichondrium), and interstitial growth occurs "in the middle" of the mass of cartilage. As a general rule then, interstitial growth is responsible for increases in size overall, and appositional growth adds various protuberances that eventually are going to be replaced by bone to create the final shape of the structure. But the two are in essence the same thing, and completely complementary to each other. They occur simultaneously and in a completely coordinated manner.

Interstitial growth is the result of chondrocytes in their lacunae actively synthesizing matrix material. This causes the total volume of the cartilaginous structure to increase. Overall growth of the structure mainly occurs in this way.

Appositional growth occurs when the "chondrogenic" cells of the perichondrium (i.e., the cells in the overlying CT that have the potential to become chondrocytes) gear up, begin active synthesis, and start creating new cartilage at the boundaries of the structure. Eventually these new chondrocytes will become trapped in lacunae and become integrated as part of the main mass of cartilage. At that point, if they're still active in synthesis, they'll be participating in interstitial growth. By controlling the rate of interstitial versus appositional growth, the shape of the cartilaginous structure can be changed.

* [Title] mTOR signaling contributes to chondrocyte differentiation.
* The mammalian Target Of Rapamycin (mTOR) is a nutrient-sensing protein kinase that regulates numerous cellular processes.
* Fetal rat metatarsal explants were used as a physiological model to study the effect of mTOR inhibition on chondrogenesis.
* Rapamycin significantly diminished this response to insulin through a selective effect on the hypertrophic zone.
* Cell proliferation (bromodeoxyuridine incorporation) was unaffected by rapamycin.
* Similar observations were made when rapamycin was injected to embryonic day (E) 19 fetal rats in situ.
* In the ATDC5 chondrogenic cell line, rapamycin inhibited proteoglycan accumulation and collagen X expression.
* Rapamycin decreased content of Indian Hedgehog (Ihh), a regulator of chondrocyte differentiation.
* Addition of Ihh to culture medium reversed the effect of rapamycin.
* We conclude that modulation of mTOR signaling contributes to chondrocyte differentiation, perhaps through its ability to regulate Ihh.
* Our findings support the hypothesis that nutrients, acting through mTOR, directly influence chondrocyte differentiation and long bone growth.